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Acta Biochimica et Biophysica Sinica Advance Access originally published online on July 30, 2009
Acta Biochimica et Biophysica Sinica 2009 41(9):745-753; doi:10.1093/abbs/gmp063
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

Hyperlipidemia does not prevent the cardioprotection by postconditioning against myocardial ischemia/reperfusion injury and the involvement of hypoxia inducible factor-1{alpha} upregulation

Huanxin Zhao1,2,4, Yehong Wang1, Ye Wu1, Xiaoyu Li1, Guangzhao Yang1, Xiurui Ma1, Rongrui Zhao1,2 and Huirong Liu2,3,*

1 Department of Physiology, Shanxi Medical University, Taiyuan 030001, China
2 Key Laboratory of Cellular Physiology, Shanxi Medical University, Chinese Education Ministry, Taiyuan 030001, China
3 School of Basic Medical Sciences, and Cardiovascular Research Institute, Capital Medical University, Beijing 100069, China
4 Shanxi College of Traditional Chinese Medicine, Taiyuan 030012, China

* Correspondence address. Tel: +86-351-4135076; Fax: +86-351-4135076; E-mail: liuhr2000{at}126.com


  Abstract

Hyperlipidemia is regarded as an independent risk factor in the development of ischemic heart disease, and it can increase the myocardial susceptibility to ischemia/reperfusion (I/R) injury. Ischemic postconditioning (Postcon) has been demonstrated to attenuate the myocardial injury induced by I/R in normal conditions. But the effect of ischemic Postcon on hyperlipidemic animals is unknown. Hypoxia inducible factor-1 (HIF-1) has been demonstrated to play a central role in the cardioprotection by preconditioning, which is one of the protective strategies except for Postcon. The aim of this study was to determine whether Postcon could reduce myocardial injury in hyperlipidemic animals and to assess whether HIF-1 was involved in Postcon mechanisms. Male Wistar rats underwent the left anterior descending coronary occlusion for 30 min followed by 180 min of reperfusion with or without Postcon after fed with high fat diet or normal diet for 8 weeks. The detrimental indices induced by the I/R insult included infarct size, plasma creatine kinase activity and caspase-3 activity. Results showed that hyperlipidemia remarkably enhanced the myocardial injury induced by I/R, while Postcon significantly decreased the myocardial injury in both normolipidemic and hyperlipidemic rats. Moreover, both hyperlipidemia and I/R promoted the HIF-1{alpha} expression. Most importantly, we have for the first time demonstrated that Postcon further induced a significant increase in HIF-1{alpha} protein level not only in normolipidemic but also in hyperlipidemic conditions. Thus, Postcon reduces the myocardial injury induced by I/R in normal and hyperlipidemic animals, and HIF-1{alpha} upregulation may involve in the Postcon-mediated cardioprotective mechanisms.

Keywords    hyperlipidemia; ischemic postconditioning; myocardial infarction; hypoxia inducible factor-1

Received: March 10, 2009; Accepted: June 1, 2009
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